FAT ENERGY Flashcards
sources of fat during exercise
intramscular triglycerides: primary source in high intensity
- trained individuals use muscle more effectively
plasma FFA: from adipose tissue lipolysis
- triglycerides –> FFA + glycerol
- low intensity
- important as musc glycogen lvls decline
- subcutaneous fat
lipolysis
breaking down of triglycerides via lipase enzymes
TGs are only useful fat for energy
how many carbons in FFAs
varies
this is why ATP produced via beta oxidation varies
main triglyceride sources
- adipocytes: fat storage across body via adipose tissue cells
- intramuscular TG
- blood lipoproteins: form of cholesterol i.e. HDL, LDL
6 stages of lipid breakdown
- mobilization
- transport
- uptake
- activation
- beta-oxidation
- mitochondrial oxidation
mobilization
triglyceride breakdown
hormone sensitive lipase: aka HSL
- ATP input needed for adipose and muscle activation
lipoprotein lipase: LPL
***ATP cleaves FFA off, which are then transported to muscle for energy
- 1 ATP/FFA
- remaining glycerol goes to liver to become glucose
transport
FFA circulates in blood by binding to ALBUMIN carrier protein
- bcs hydrophobic
in cells, FAs are activated via carnitine transferase…then transported across cell membrane into mitochondria for oxidation
uptake
active transport into muscle cytosol
special transport proteins used to move FFA
activation
prepare for breakdown
coa is added to FFA…becomes fatty acyl-coa
- this requires ATP
then moves across membrane into mitochondria via carrier
during b-oxidation, acyl coa is cleaved off
beta-oxidation
FFA is broken down in mitochondria
acyl coa dehydrogenase makes FAD –> FADH2
b-hydroxyacyl coa dehydrogenase makes NAD –> NADH
produces fatty acl coa, which is recycled to continue b-oxidation
also makes acetyl coa, which goes to krebs
mitochondrial oxidation
b-oxi products go to TCA and ETC
FADH2 and NADH go to ETC
acetyl coa goes to krebs
rule for b-oxi cycles and FAs
c/2 - 1 = number of cycles i.e. 7
of carbons is important i.e. 16c
of acetyl coa = #c/2 i.e. 8
b-oxi cannot occur with 2 carbons
products of b-oxi
each cycle makes:
1 NADH
1 FADH2
1 acetyl coa (3 NADH, 1 FADH, 1 ATP)
total 14 ATP
net = 12 ATP (2 invested to acquire FA)
2 invested PER fatty acid
- i.e. for 3 FAs, subtract 6 ATP
what does glycerol do after it’s cleaved from TG
can be used as energy source
- converted to form the liver can use for glycolysis
- does NOT contribute during exercise
1 ATP used to phosphorylate glycerol to G3P
- also reduces NAD –> NADH
- proceeds to glycolysis, making pyruvate
glycerol metabolism
glycerol –> G3P
2 ATP + 2 NADH + acetyl coa (3 nadh, 1 fadh, 1 atp)
1 glycerol = 17 ATP
net = 16
what about protein
contributes very little
has nitrogen, even more steps to become energy
not often used
carb vs fat
carb: limited stores
fat: almost unlimited
carb 20% more efficient, allows exercise at high intensity
- faster rate, less o2 use
when do energy systems contribute
phosphagen 10 seconds
anaerobic 1-2mins
equal by 75s
aerobic dominates after 2 minutes
which system dominates at rest
aerobic, almost 100% ATP
MET
metabolic equivalent of a task
1 MET = 3.5ml/kg/min
- resting o2 consumption
is relative to person’s musc mass
vo2
volume of o2 consumed/minute
L/min is absolute value
ml/kg/min when divide by body weight…allows to compare size/BW effectively
the larger the person, the higher the absolute vo2
rest-to-exercise transition
ATP production immediately increases
o2 uptake rapid inc, but NOT instantaneous
steady state w/in 1-4 mins after ATP requirement is met thru aerobic metabolism
o2 deficit vs o2 debt
o2 deficit: lag in o2 uptake at beginning of exercise
o2 debt: repayment for o2 deficit at onset of exercise
- original term for EPOC
recovery from exercise
o2 uptake remains elevated above rest
EPOC: excess post-exercise oxygen consumption
- repayment for o2 deficit
- separated by rapid and slow phase
rapid vs slow phase EPOC
rapid phase: steep decline in vo2 (consumption) post-exercise
- 2-3mins
- o2 needed to resynthesize ATP and PCr, and replace tissue stores of o2
- 20% EPOC
slow phase: 30 minutes post exercise, slow dec in o2 consumption
why o2 is still elevated after exercise:
1. gluconeogenesis from lactate
2. HR and breathing elevated
3. elevated blood temp
4. elevated hormone concentration
5. others: glycogen depletion, ph restoration, uncoupling ATP
comparing trained vs untrained EPOC and lactate
trained: lower o2 deficit, better developed aerobic capacity
- bcs of CV and musc adaptations
- less lactate and H production
- faster o2 uptake via offloading to muscles
fate of lactate
used as fuel for heart and brain
- becomes acetyl-coa
oxidized in other tissues 60%
forms glucose in liver and stores as glycogen 25%
forms proteins 15%
excreted
lactate shuttle
lactate is produced in one tissue and moves to another
bcs lactate is an important cell signal/fuel
- originally thought as waste
how does lactate become glucose
by the cori cycle in the liver
cori cycle
lactate produced by muscle and is transported to liver
- a lactate shuttle
in liver, lactate becomes glucose via gluconeogenesis
glucose transports to muscle, where it’s used in glycolysis
lactate threshold
point where blood lactate concentration rises systematically during incremental exercise
- aka pt where lactate accumulates
- also called anaerobic threshold
when blood lactate lvls are 1mmol/L GREATER than resting values
no longer able to handle lactate production rate
- if continue, become fatigued
trained ppl reach threshold later, closer to VO2 max
OBLA
onset of blood lactate accumulation
when blood lactate lvls reach 4mmol/L
- not above rest
- begins to accumulate at more accelerated rate
train to perform at this lvl for as long as possible
what causes ppl to reach lactate threshold faster
low musc o2
accelerated glycolysis, produces more lactate
recruitment of fast twitch fibres: fatiguable
reduced lactate removal
LDH isozyme: catalyzes lactic acid + LDH –> lactate
why do we measure lactate threshold
- training status
- predicts endurance performance
- establishes training intensity…program to inc threshold
specificity of OBLA
characterized by exercise task specificity
diff exercise modes CANNOT have interchangeable OBLA
i.e. cannot compare running to cycling
crossover concept
shift from fat to carb as intensity increases
due to recruitment of fast twitch fibres and inc blood levels of epinephrine
